Approach to Seizures 
  • A seizure is a paroxysmal event due to abnormal, excessive, hypersynchronous discharges from an aggregate of central nervous system (CNS) neurons. 
  • Epilepsy describes a condition in which a person has recurrent seizures due to a chronic, underlying process. i.e. 2 or more episodes of seizures. 
  • Partial (or focal) seizures 
    1. Simple-partial seizures do not affect consciousness and may have motor, sensory, autonomic, or psychiatric symptoms. 
    2. Complex-partial seizures include alteration in consciousness coupled with automatisms (e.g., lip smacking, chewing, aimless walking, or other complex motor activities). 
  • Generalized seizures 
    1. Involve diffuse regions of the brain in a bilateral symmetric fashion 
    2. May occur as a primary disorder or may result from secondary generalization of a partial seizure 
    3. Tonic-clonic seizures (grand mal) 
      • Sudden loss of consciousness 
      • Loss of postural control 
      • Tonic muscular contraction producing teeth-clenching and rigidity in extension (tonic phase), followed by rhythmic muscular jerking (clonic phase) 
    4. Absence seizures (petit mal) 
      • Sudden, brief impairment of consciousness without loss of postural control 
    5. Other types of generalized seizures are atypical absence, infantile spasms, tonic, atonic, and myoclonic seizures. 
Seizures result from a shift in the normal balance of neuronal excitation and inhibition.  
The most common causes are perinatal hypoxia and ischemia, intracranial hemorrhage and trauma, Acute CNS infection, Metabolic disturbances , Drug withdrawal, Developmental disorders, Genetic disorders, Febrile seizures ,Trauma, Brain tumor, Illicit drug use, Alcohol withdrawal, Cerebrovascular disease, sleep deprivation and Drugs.  
Symptoms & Signs 
  • Preceding aura : A subjective sensation, often of anxiety, an odd smell or taste, or some minor motor phenomena (e.g., twitching) just before the seizure occurs 
  • Headache 
  • Alterations in consciousness (from confusion to unresponsiveness) : Automatisms such as Lip smacking, Chewing and  Aimless walking 
  • Tonic muscular contraction producing teeth-clenching and rigidity in extension (tonic phase), followed by rhythmic muscular jerking (clonic phase) 
  • Loss of postural control 
  • Tongue biting 
  • Bowel and bladder Incontinence 
  • Autonomic symptoms such as tachycardia, hypertension, pupillary dilation 
  • In status epilepticus, patients may have only subtle mild clonic movements of the fingers, or fine, rapid movements of the eyes. There may also be associated paroxysmal episodes of autonomic changes such as hypertension, tachycardia, and pupillary changes. 
  • In nonconvulsive status epilepticus in an unresponsive patient, there may be no clinical signs of ongoing seizure activity. (If a pt. has a severe change in mental status, it could be post ictal confusion or ongoing status epilepticus, which can only be found by EEG).  TODD’s Palsy is usually unilateral weakness following the seizure, which resolves in 48 hrs. It may also affect speech, gaze and vision. 
  • Seizures can cause direct neuronal injury from excitotoxicity. 
Differential Diagnosis 
  • Syncope 
    • A syncopal episode is more likely if the event was provoked by acute pain or anxiety or occurred immediately after arising from the lying or sitting position. 
    • Patients with syncope often describe a stereotyped transition from consciousness to unconsciousness that includes tiredness, sweating, nausea, and tunneling of vision. 
    • Loss of consciousness with syncope is usually very brief, without post-event sleepiness (i.e., typically a prolonged postictal state is absent). 
    • Loss of consciousness with syncope can be associated with brief myoclonic jerking that is often misinterpreted as rhythmic clonic seizure activity. 
  • Psychological disorders 
    • Psychogenic seizure (nonepileptic seizures) 
    • Psychogenic seizures often last longer than epileptic seizures and may wax and wane over minutes to hours.  
    • Hyperventilation 
    • Panic attack 
    • Video EEG monitoring is often useful when historic features are not present. 
  • Metabolic disturbances 
    • Alcoholic blackouts 
    • Delirium tremens 
    • Hypoglycemia 
    • Hypoxia 
    • Psychoactive drugs (e.g., hallucinogens) 
  • Migraine 
    • Confusional migraine 
    • Basilar migraine 
  • Transient ischemic attack (TIA) : Basilar artery TIA 
  • Sleep disorders 
    • Narcolepsy/cataplexy 
    • Benign sleep myoclonus 
  • Movement disorders 
    • Tics 
    • Nonepileptic myoclonus 
    • Paroxysmal choreoathetosis 
Diagnostic Approach 
  • When a patient presents shortly after a seizure, the first priorities are:  
    • Attention to vital signs 
    • Respiratory and cardiovascular support 
    • Treatment of seizures if they resume 
  • Life-threatening conditions must be diagnosed and managed appropriately. Dig into the causes of seizure and what precipitated the seizures?  
  • If this is the first seizure, emphasis will be on: 
    • Establishing whether the reported episode was a seizure rather than another paroxysmal event. 
    • Determining the cause of the seizure by identifying risk factors and precipitating events. 
    • Identifying, if possible, if the seizure was focal or generalized in onset, as this is important for directing further workup and selecting appropriate anticonvulsant therapy  
  • Precipitating factors such as sleep deprivation, systemic diseases, electrolyte or metabolic derangements, and acute infection should be identified. 
  • Many prescription medications, including quinolone antibiotics, antipsychotic agents, and antidepressants, may also lower seizure threshold.  
Laboratory Tests 
  • Blood glucose 
  • Routine blood studies CBC, BMP, LFT, Ammonia, to identify the causes of seizures 
  • Toxin screen in blood and urine 
  • Therapeutic drug levels 
  • Serum prolactin levels: Most generalized seizures and many complex partial seizures are accompanied by rises in serum prolactin (during the immediate 30-minute postictal period); psychogenic seizures are not. May discriminate between organic and psychogenic seizures. Should not be used as a test for status epilepticus. 
  • Brain imaging recommended for all patients with unexplained new-onset seizures to search for an underlying structural abnormality. 
  • MRI has been shown to be superior to CT for the detection of cerebral lesions associated with epilepsy except hemorrhagic lesions. 
  • In the patient with a suspected CNS infection or mass lesion, CT scanning should be performed emergently when MRI is not immediately available. 
Diagnostic Procedures 
  • EEG 
    • All patients who have a possible seizure disorder should be evaluated with an EEG. 
    • EEG measures electrical activity of brain by recording from electrodes placed on the scalp. The absence of electrographic seizure activity doesn’t exclude a seizure disorder. Simple or complex seizures may originate from a region of cortex that is beyond range of the scalp electrodes. When a routine EEG is unrevealing and seizures remain a diagnostic concern, prolonged recording with an ambulatory EEG recording device or with inpatient continuous video and EEG monitoring can be considered.  
    • EEG should be performed to rule out ongoing status epilepticus in patients who remain comatose after seizure. 
  • Lumbar puncture 
    • Indicated if there is any suspicion of meningitis or encephalitis 
    • Mandatory in all patients infected with HIV, even in the absence of symptoms or signs suggesting infection 
  • Partial seizures 
    1. Simple-partial seizures (with motor, sensory, autonomic, or psychiatric signs) 
    2. Complex-partial seizures 
    3. Partial seizures with secondary generalization 
  • Primarily generalized seizures 
    1. Absence (petit mal) 
    2. Tonic-clonic (grand mal) 
    3. Tonic 
    4. Atonic 
    5. Myoclonic 
Treatment Approach 
Single seizure or recurrent seizures due to correctable or avoidable circumstances are not necessarily epilepsy. 
  • Identify and treat any life-threatening conditions: CNS infection, metabolic derangement, or drug toxicity. 
  • Identify underlying cause and precipitating factors. Antiepileptic therapy is usually unnecessary unless the metabolic disorder cannot be corrected promptly.  
  • Initial laboratory studies: complete blood count, electrolytes, calcium, magnesium, glucose, liver and renal function, urinalysis, and toxicology screen 
  • MRI or EEG if no metabolic cause 
Drug therapy: initiation, monitoring, and titration 
  • Start with lowest typical dose to minimize side effects. 
  • Buproprion should be avoided in patients with epilepsy due to adverse effects on seizure control.  
  • Patients with abnormal results on EEG or head MRI are at high risk for recurrent seizure and should be placed on an antiepileptic drug. In patients whose EEGs and MRIs are normal, the 2-year recurrence risk after a first seizure has been shown to be approximately 40%; unless special circumstances exist, medication is generally not started for these patients.  
  • Subsequent increase in dosage only after interval of 5 or more half-lives 
    • Key determinants for dosing: seizure frequency and side effects, not laboratory values. Monitoring drug level may be useful to establish initial dosing schedule. 
    • Therapeutic ranges are only an approximate guide. In subtherapeutic drug levels, adjust dose only if seizures remain uncontrolled. 
    • Determination of optimal dose is often trial and error. May take months or longer if low baseline seizure frequency 
  • Patients with juvenile myoclonic epilepsy need lifelong antiepileptic therapy 
  • If seizures continue despite gradual increases to the maximum tolerated dose and documented compliance, switch to another antiepileptic drug. 
  • Maintain patient on first drug while second is added. Adjust dose of second drug to decrease seizure frequency without causing toxicity. Gradually withdraw first drug. Optimize dose of the second drug based on seizure response and side effects.  
  • Therapeutic drug monitoring 
    • Drug levels should be followed to document compliance and to adjust dosing if seizures continue despite treatment. 
    • In general, if patient is seizure-free and has no side effects from the medication, dosing levels should not be routinely adjusted simply to target a specific "therapeutic range." 
  • Withdrawal of anti-epileptics 
    • Complete medical control of seizures for 1–5 years 
    • Single seizure type, either partial or generalized 
    • Normal neurologic examination, including intelligence 
    • Normal EEG 
    • It seems reasonable to attempt withdrawal of therapy after 2 years in a patient  
    • In most cases, it is preferable to reduce drug dose gradually over 2–3 months. 
    • Most recurrences occur in the first 3 months after discontinuing therapy. 
    • Patients should be advised to avoid potentially dangerous situations such as driving or swimming during withdrawal period. 
  • Status epilepticus 
  • Postictal (Todd’s) paralysis 
  • Seizure-related trauma (e.g. tongue lacerations, posterior shoulder dislocations) 
  • Increased mortality 
  • Memory loss 
  • Psychiatric problems 
  • Psychosocial complications 
Status Epilepticus 
A state of continuous seizures or repetitive, discrete seizures with impaired consciousness in the interictal period.  Typically, convulsions > 5 mins in duration or 2 or more seizure episodes without a return to baseline. It can be:  
  • Generalized convulsive status epilepticus (GCSE) (e.g., persistent, generalized electrographic seizures, coma, and tonic-clonic movements) 
  • Nonconvulsive status epilepticus (e.g., persistent absence seizures or partial seizures, confusion, impaired consciousness, and minimal motor abnormalities) 
Duration:  Traditional criterion: 15–30 minutes but Practical criterion is prompting acute use of anticonvulsant therapy; for GCSE this is typically > 5 minutes. 
Physiological changes: 
  1. Initial stage  
    • Cerebral metabolism is greatly increased because of seizure activity, but physiologic mechanisms are sufficient to meet the metabolic demands. 
    • Cerebral: increased blood flow, increased metabolism 
    • Autonomic and cardiovascular: hypertension, increased cardiac output, massive catecholamine release, tachycardia, arrhythmias, hyperpyrexia and acidosis 
    • Metabolic: lactic acidosis, hyperglycemia 
  2. Decompensated phase 
    • Cerebral metabolic demands cannot be fully met, resulting in hypoxia and altered cerebral and systemic metabolic patterns. 
    • Cerebral: hypoxia, hypoglycemia, increased intracranial pressure 
    • Autonomic and cardiovascular: hypoxia, hypotension, hyperpyrexia 
    • Metabolic: hypoglycemia, hyponatremia, hyperkalemia, metabolic acidosis 
Symptoms & Signs 
  • Overt convulsions 
  • After 30–45 minutes of uninterrupted seizures, signs may become increasingly subtle. 
    • Mild clonic movements of only the fingers 
    • Fine, rapid movements of the eyes 
    • Paroxysmal episodes of tachycardia, hypertension, and pupillary dilation 
Differential Diagnosis 
  • Coma : After overt seizures, if patient remains comatose, EEG should be obtained to evaluate for ongoing nonconvulsive SE. 
  • Nonepileptic Status epilepticus: May occur in patient with psychogenic nonepileptic seizures 
Laboratory Tests 
  • Anticonvulsant levels 
  • Creatine phosphokinase 
  • Serum osmolality 
  • Liver and renal function tests 
  • Toxicology tests: blood and urine 
  • Arterial blood gas 
  • Carboxyhemoglobin 
  • Cardiorespiratory dysfunction : Hypoxia , aspiration pneumonia ,arrhythmia, high-output cardiac failure 
  • Hyperthermia 
  • Metabolic derangements : Lactic acidosis , hyponatremia , hyperkalemia , hypoglycemia and hypercapnia 
  • Acute renal failure due to rhabdomyolysis 
  • Profound CNS injury can occur when the patient is paralyzed with neuromuscular blockade but continues to have electrographic seizures. 
  • Irreversible neuronal injury 
  • Death 
Treatment protocol: general measures 
  • Assess carefully for evidence of respiratory or cardiovascular insufficiency. 
  • With careful monitoring and standard airway protection, patients usually do not require intubation (if intubation is necessary, use short-acting paralytics). 
  • Establish intravenous access and administer: 
    • Thiamine 100 mg before giving glucose 
    • 50% dextrose in water 50 mL 
    • Naloxone 0.4 mg  
Treatment protocol: anticonvulsant therapy 
  • Lorazepam (0.1 mg/kg IV upto a maximum of 4mg over 1–2 min; repeat x 1 if no response after 5 minutes) i.e. can give ATIVAN upto 10 mg in single dose. 
  • If seizures continue 
    1. For patients taking valproate whose level may be subtherapeutic: Consider valproate 25 mg/kg IV. 
    2. Phenytoin (20 mg/kg IV at 50 mg/min) or fosphenytoin (20 mg/kg  at 150 mg/min) 
    3. Fosphenytoin has a peak serum level within six minutes after intravenous loading 
    4. Monitor blood pressure; electrocardiogram; and, if possible, EEG during infusion. 
    5. Side effects: Phenytoin can cause precipitous fall in blood pressure if given too quickly, especially in elderly patients. 
    6. If seizures are not controlled, continue phenytoin at 7–10 mg/kg IV at 50 mg/min or fosphenytoin at 7–10 mg/kg PE IV at 150 mg/min. 
  • If seizures continue 
    1. Consider valproate 25 mg/kg IV followed by 500mg Q6hrs 
    2. Lacosamide 500mg followed by 200-300mg Q12 
    3. Keppra  (20mg/kg) 1gm- 2gm IV followed by 500mg -1000mg Q12hrs 
  • If seizures continue and no immediate access to ICU 
    • May add phenobarbital (20 mg/kg IV at 60 mg/min) 
    • If seizures continue: phenobarbital (10 mg/kg IV at 60 mg/min) 
  • If seizures continue, admit to ICU for anesthesia with midazolam, propofol, ketamine (down regulates GABA receptors) or pentobarbital 
  • If IV access is not immediately available , can use rectal diazepam  or intramuscular, nasal or buccal midazolam  
Generalized Epilepsy 
Generalized epilepsy is a chronic seizure disorder characterized by seizures that arise from simultaneous activation of diffuse regions of both cerebral hemispheres. 
Generalized seizure classification includes: 
  • Absence seizures (petit mal)Sudden, brief lapse of consciousness without loss of postural control 
  • Generalized tonic-clonic seizures (grand mal) Sudden loss of consciousness followed first by generalized muscular contraction (tonic phase) and second by superimposed periods of muscular relaxation that cause the body to jerk rhythmically (clonic phase) 
  • Tonic seizures : Only the tonic phase occurs. 
  • Clonic seizuresOnly the clonic phase occurs. 
  • Atonic seizures Sudden, brief loss of postural muscle tone with brief impairment of consciousness 
  • Myoclonic seizuresSudden, brief muscular contractions 
Symptoms & Signs 
Absence seizures (petit mal) 
  • Characterized by sudden, brief lapses of consciousness without loss of postural control 
  • Seizure typically lasts for only seconds; consciousness returns as suddenly as it was lost; no postictal confusion. Seizures can occur hundreds of times per day; patient may be unaware of or unable to convey their existence. 
  • Unexplained "daydreaming" or decline in school performance recognized by a teacher 
  • Usually accompanied by subtle, bilateral motor signs such as rapid blinking of the eyelids, chewing movements, or small-amplitude clonic movements of the hands 
Generalized tonic-clonic seizures (grand mal) 
  • Most common seizure type in metabolic derangements; frequently encountered in many different clinical settings.  
  • Initial phase of seizure manifests as tonic contraction of muscles throughout the body. Tonic contraction of muscles of expiration and larynx at onset produces a loud moan or "ictal cry." Respirations are impaired; secretions pool in the oropharynx; cyanosis develops. Contraction of the jaw muscles may cause biting of the tongue.  There is a marked enhancement of sympathetic tone with increase in heart rate, blood pressure, and pupillary size  
  • After 10–20 seconds, the tonic phase of the seizure evolves into the clonic phase (the superimposition of periods of muscle relaxation on the tonic muscle contraction). 
  • Periods of relaxation progressively increase until the end of the ictal phase, which usually lasts no more than 1 minute. 
  • Postictal phase is characterized by unresponsiveness, muscular flaccidity, and excessive salivation that can cause stridorous breathing and partial airway obstruction. 
    • Bladder or bowel incontinence may occur. 
    • Gradual regaining of consciousness over minutes to hours 
    • Postictal confusion 
    • Headache, fatigue, and muscle ache may last for many hours. 
    • Postictal phase may last many hours in patients with prolonged seizures or underlying CNS diseases (e.g., alcoholic cerebral atrophy). 
Atonic seizures 
  • Characterized by sudden loss of postural muscle tone lasting 1–2 seconds 
  • Consciousness is briefly impaired; usually there is no postictal confusion. 
Myoclonic seizures 
  • Myoclonus is a sudden and brief muscle contraction that may involve 1 part or entire body. This is the only generalized epilepsy that won’t cause loss of consciousness.  Normal, common physiologic form is sudden jerking movement while falling asleep. Pathologic myoclonus is associated with metabolic disorders, degenerative CNS diseases, or anoxic brain injury 
  • Considered to be true epileptic events; are caused by cortical dysfunction 
  • Usually coexist with other forms of generalized seizure disorders 
Focal Epilepsy 
Symptoms & Signs 
Simple partial seizures 
  • Motor, sensory, autonomic, or psychic symptoms occur without alteration in consciousness. 
  • Involuntary movement on contralateral side (focal motor seizure) 
    • Movements are typically clonic (i.e., repetitive, flexion/extension movements)  
    • Jacksonian march: Abnormal motor movements begin in a restricted region and gradually progress (over seconds to minutes) to include a larger portion of the body (e.g., begins in face, gradually involves arm and then leg). 
    • Todd’s paralysis: Localized, post-seizure paresis persists for minutes to many hours in the involved region. Usually resolves in 48 hours. 
  • Changes in somatic sensation (e.g., paresthesias), vision (flashing lights or formed hallucinations), equilibrium (sensation of falling or vertigo), or autonomic function (flushing, sweating, piloerection) 
  • Seizures arising from the temporal or frontal cortex may cause alterations in hearing, olfaction, gustatory or higher cortical function (psychic symptoms such as déjà- Vu). 
  • Psychic symptoms such as fear, sense of impending change, detachment, depersonalization, déjà vu, or illusions that objects are growing smaller (micropsia) or larger (macropsia) 
Complex partial seizures  
  • Focal seizure activity accompanied by transient inability to interact with the environment 
    • Consciousness is impaired, not lost. Confusion typically follows seizure. Recovery of consciousness ranges from seconds to an hour. Patient may also have Anterograde amnesia.  
    • Inability to respond appropriately to visual or verbal commands and Impaired recollection or awareness of ictal phase 
    • Frequently with aura stereotypic for patient 
  • Ictal phase often starts with sudden behavioral arrest or motionless stare; onset of amnesia. 
  • Automatisms (involuntary, automatic behaviors) usually accompany behavioral arrest. 
  • Basic behaviors: chewing, lip smacking, swallowing, or "picking" movements of the hands 
  • Elaborate behaviors: emotional display, running 
Partial seizures with secondary generalization 
  • Partial seizures can spread to involve both cerebral hemispheres and produce a generalized seizure, usually tonic-clonic.  
  • Often difficult to distinguish from a primarily generalized tonic-clonic seizure. Focal onset of the seizure may become apparent with careful history (e.g., report of a stereotypical aura) or electroencephalogram (EEG) (e.g., focal area of epileptiform activity). 
Anti epileptics
First-line agents- Valproate, phenytoin, keppra, lamotrigine and topiramate 
Valproic acid 
  • Best initial choice in primarily generalized tonic-clonic seizures and absence seizures
  • Typical dose; dose interval: 750–2000 mg/d in bid–qid doses 
  • Therapeutic range: 50–150 μg/mL 
  • Metabolised by liver
  • Adverse effects are ataxia, sedation, tremor, hepatotoxicity, thrombocytopenia, GI irritation, weight gain, transient alopecia, hyperammonemia 
  • Tonic-clonic and focal-onset seizures : Can worsen certain types of generalized seizures, including absence-, myoclonic-, tonic-, and atonic seizures 
  • Typical dose; dose interval: 300–400 mg/d ; qd–tid 
  • Therapeutic range: 10–20 μg/mL 
  • Adverse effects are dizziness, diplopia, ataxia, incoordination, confusion, gum hyperplasia, lymphadenopathy, hirsutism, osteomalacia, facial coarsening, skin rash 
  • Recommended as adjunctive therapy only; can’t use for absence seizures. 
  • Typical dose; dose interval: 1000–3000 mg/d as bid dosing. Half-life: 6–8 hours
  • Excreted by kidneys
  • Recommended as adjunctive therapy only
  • Typical dose; dose interval: 200–400 mg/d; qd–bid 
  • Half-life: 50–68 hours 
  • Tonic-clonic and focal-onset seizures 
  • Typical dose; dose interval: 600–1800 mg/d (15–35 mg/kg, child); bid–qid 
  • Therapeutic range: 6–12 μg/mL 
  • Adverse effects are ataxia, dizziness, diplopia, vertigo , aplastic anemia, leukopenia, GI irritation, hepatotoxicity, hyponatremia 


  • Effective in epilepsy syndromes with mixed, generalized seizure types (e.g., JME and Lennox-Gastaut syndrome) 
  • Typical dose; dose interval: 150–500 mg/d; bid 
  • Focal-onset seizures, tonic-clonic seizures, and Lennox-Gastaut syndrome 
  • Typical dose: dose interval: 200–400 mg/d; bid 
  • Adverse effects are psychomotor slowing, sedation, speech or language problems, fatigue, paresthesias , renal stones , weight loss 
Alternative/adjunctive agents- phenytoin, carbamazepine, phenobarbitone, primidone, zonisamide 
  • Focal-onset and similar to carbamazepine 
  • Typical dose; dose interval: 900–2400 mg/d (30–45 mg/kg, child); bid 
  • Typical dose; dose interval: 60–180 mg/d ; qdaily 
  • Therapeutic range: 10–40 μg/mL 
  • Adverse effects are sedation, ataxia, confusion, dizziness, decreased libido, depression 
  • most useful in absence seizures; not useful for tonic-clonic or partial seizures 
  • Typical dose; dose interval: 750–1250 mg/d (20–40 mg/kg); qd–bid 
  • Indicated for Absence, atypical absence, and myoclonic seizures 
  • Typical dose; dose interval: 1–12 mg/d (0.1–0.2 mg/kg); qd–tid 
  • Typical dose; dose interval: 900–2400 mg/d; tid–qid 
Treatment of refractory epilepsy 
  • Initial combination therapy usually combines first-line drugs. If unsuccessful, add topiramate or levetiracetam. 
  • For myoclonic seizures resistant to valproic acid, add clonazepam. 
  • Absence seizures may respond to combination of valproic acid and ethosuximide. 
  • Vagus nerve stimulation : Option in medically refractory epilepsy if resective brain surgery not possible 
  • Epilepsy Surgery: Patients who have undergone two medication trials without success are appropriately referred to a specialized epilepsy center for surgical evaluation. The goal of epilepsy surgery is to remove the area of cortex from which seizures are generated 
  • All women of childbearing age taking anticonvulsant medications should be counseled about the need to take daily folate (to decrease the risk of neural tube defects) and to consider alternative forms of birth control (as most anticonvulsants decrease effectiveness of oral contraceptives). 
  • Patients with temporal lobe epilepsy refractory to trials of 2 or more medications are unlikely to achieve adequate control with further trials of anticonvulsant combinations, and temporal lobectomy should be considered early in these patients. 
  • After a single unprovoked seizure, a greater risk of recurrence is predicted by a partial seizure, Todd paralysis, a family history of epilepsy, age greater than 65 years, and abnormal findings on neurologic examination.  
  • Unexplained unresponsiveness following resolution of a generalized seizure suggests ongoing seizure activity (nonconvulsive status epilepticus), often detectable only by EEG monitoring. 
  •  In general, if patients with epilepsy are seizure-free and without side effects on a given anticonvulsant regimen, doses should not be adjusted simply to target a specific "therapeutic range." A therapeutic dose is one that prevents seizures without causing side effects. 
  • Chronic use of first-generation antiepileptic drugs has been associated with increased risk of osteoporosis and vitamin D deficiency. 
  • Phenobarbital, phenytoin, carbamazepine, and oxcarbamazepine all induce hepatic cytochrome P450 enzymes, and valproic acid inhibits them. 
  • Dilantin level should be corrected in both hypoalbuminemia and renal failure, if GFR<20. 
  • EEG should be the opposite of the ECG:  
    • the more the EEG looks like VF, the better it is. 
    • the more the EEG looks like sinus rhythm, the worse it is 
    • the more the EEG varies in frequency and amplitude over time, the better it is. 

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